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Metabolic alterations in the chronically denervated dog heart
G J van der Vusse1, M L Dubelaar, W A Coumans
1Department of Physiology, Maastricht University, Netherlands. vandervusse@fys.unimaas.nl
Cardiovascular Research
|April 16, 1998
Summary
Chronic cardiac denervation impairs myocardial glucose oxidation due to decreased active pyruvate dehydrogenase. This study investigated glucose transporters, enzymes, and fatty acid handling proteins in denervated dog hearts.
Area of Science:
- Cardiovascular Physiology
- Metabolic Biochemistry
Background:
- Chronic cardiac denervation is known to impair myocardial glucose oxidation.
- Left ventricular efficiency decreases following chronic cardiac denervation.
Purpose of the Study:
- To investigate alterations in glucose transporters, glycolytic enzymes, and pyruvate dehydrogenase activity after chronic cardiac denervation.
- To examine if changes in fatty acid handling proteins or mitochondrial properties contribute to impaired glucose utilization and reduced cardiac efficiency.
Main Methods:
- Adult dogs underwent chronic cardiac denervation via surgical ablation of extrinsic nerve fibers or sham operation.
- Left ventricular biopsies were analyzed for glucose and fatty acid handling proteins and enzyme activity.
- Mitochondrial glutamate oxidation was assessed.
Main Results:
- GLUT1 transporter content increased in the denervated left ventricle.
- The active form of pyruvate dehydrogenase significantly declined (p < 0.05).
- Fatty acid handling proteins and mitochondrial glutamate oxidation remained unaffected.
Conclusions:
- Impaired myocardial glucose oxidation after chronic denervation is primarily attributed to reduced active pyruvate dehydrogenase.
- Alterations in mitochondrial properties are unlikely to be the cause of decreased left ventricular work efficiency.